Akaike Masashi, Matsumoto Toshio
Tokushima University Hospital, Department of Internal Medicine, Division of Cardiology.
Clin Calcium. 2007 Jun;17(6):864-70.
Glucocorticoid excess enhances superoxide-induced inactivation of nitric oxide (NO) and suppresses NO production through decreasing the expression of endothelial NO synthase. Glucocorticoid-induced decrease in NO bioavailability elicits vasuclar endothelial dysfunction, leading to insufficiency of peripheral circulation, which may be the pathogenesis for idiopathic osteonecrosis of the femoral head (ION) . Glucocorticoid-induced vascular endothelial dysfunction is the major therapeutic target for ION. NO causes overproduction of reactive oxygen species.
糖皮质激素过量会增强超氧化物诱导的一氧化氮（NO）失活，并通过降低内皮型一氧化氮合酶的表达来抑制NO生成。糖皮质激素诱导的NO生物利用度降低会引发血管内皮功能障碍，导致外周循环不足，这可能是股骨头缺血性坏死（ION）的发病机制。糖皮质激素诱导的血管内皮功能障碍是ION的主要治疗靶点。NO会导致活性氧的过度产生。
